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ELECTROCONVULSIVE THERAPY

ELECTROCONVULSIVE THERAPY. ECT. INDICATIONS: - common -depression, schizophrenia with catatonia, schizophreniform and schizoaffective disorders - uncommon -mania, bipolar disorder, suicidal tendency, patient preference. ECT. PSYCHOPHARMACOTHERAPY:

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ELECTROCONVULSIVE THERAPY

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  1. ELECTROCONVULSIVE THERAPY

  2. ECT • INDICATIONS: • -common-depression, schizophrenia with catatonia, schizophreniform and schizoaffective disorders • -uncommon-mania, bipolar disorder, suicidal tendency, patient preference

  3. ECT • PSYCHOPHARMACOTHERAPY: • -TCA’s-amitryptyline, imipramine, nortriptyline, etc • -MAOI’s-deprenyl, phenelzine, isocarboxazid, etc • -SSRI’s-fluoxetine, etc • -Li+

  4. ECT • TCA’s: • -block reuptake of catecholamines at the presynaptic-nerve terminal and result in inc circulatory catecholamines • -inc in resting adrenergic tone • -sympathomimetic drugs (ephedrine) may result in exaggerated pressor response

  5. ECT • MAOI’s: • -block monoamine oxidase (enzyme selectively deaminates amine neuro-transmitters) • -results in accumulation in nerve terminals • -indirect sympathomimetics can precipitate HTNsive crises and direct sympatho-mimetics (neo) can have exaggerated responses • -potentiate effects of barbs (STP)

  6. ECT • LITHIUM: • -interrupts Na-K cell membrane pump and interferes with production of cAMP • -ECG changes may result • -inc Li+ levels may prolong awakening • -NMB action is prolonged

  7. ECT • MECHANISM OF ACTION: • -electrically induced grand mal sz • -stimulus is a short square wave pulse • -cellular mechanism? • -duration must be >30 sec • -CV, CNS, other physiologic effects

  8. ECT • -CVS: initial-brady, hypotension; later-tachy, dysrhythmias, ischemic changes, HTN, inc myocardial O2 consumption • -CNS: inc CBF, inc ICP, inc O2 consumption • -Other: inc IOP, inc IGP

  9. ECT • RELATIVE CONTRAINDICATIONS: • -intracranial mass lesions • -recent CVA (3 months) • -retinal detachment • -pregnancy • -long bone Fx’s • -thrombophlebitis • -acute a/o severe pulmonary disease

  10. ECT • ANESTHETIC REQUIREMENTS: • -amnesia • -airway management • -prevention of bodily harm from sz • -control of hemodynamics (B-blockers, short-acting vasodilators) • -smooth, rapid emergence

  11. ECT • -preoxygenate/airway control • -barbs, etomidate, propofol • -sux, short-acting nondep • -consider ETT if severe GERD • -additional bp cuff to isolate an arm to visually assess length of sz (>30 sec)

  12. VENOUS AIR EMBOLISM IAN LIPSKI, CA3 SUPERVISOR: DR. PIVALIZZA UTHSC AT HOUSTON: DEPT OF ANESTHESIOLOGY

  13. VAE • -may occur whenever the operative field is elevated >=5cm above the RA • -crainiotomy and spine cases • -sitting position • -also lateral, supine, prone

  14. VAE • PATHOPHYSIOLOGY: • -intense vasoconstriction of pulmonary circ which results in V/Q mismatch, interstitial pulmonary edema, inc PVR and dec CO and eventual cardiopulmonary collapse and failure • -paradoxical emboli to CNS/coronaries with PFO (20-30% pop) and RAP>LAP

  15. VAE • -MONITORING: • -TEE (most sensitive) • -precordial doppler- air as small as 0.25cc detected, R parasternal border btw 3rd and 6th intercostal spaces, high-pitched noise • -PAC- inc in PA pressures, change correlates with volume of air • -EtCO2- decreased sec to V/Q mismatching • -EtN2 (least sensitive)-increased sec to air that crosses cap-alv membrane and is exhaled

  16. VAE • -MONITORS(CONT’D): • -CVP catheter at 3 cm above jxn of SVC and RA-position confirmed by CXR or by following P wave configuration • -multi-orifice catheter better than single orifice • -entrained air can be aspirated from RA

  17. VAE • -early diagnosis of air embolism is essential for successful treatment

  18. VAE • -TREATMENT: • -flood surgical field with saline, packing and wax bone edges • -D/C N2O is utilized, 100% O2 • -lower surgical field to below heart i.e. Trendelenburg • -aspirate air from CV catheter • -compress neck veins • -supportive care: hydrate, volume expansion, pressors, etc • -PEEP/valsalva???

  19. THEEND

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